Chapter title |
Killing Is Not Enough: How Apoptosis Hijacks Tumor-Associated Macrophages to Promote Cancer Progression.
|
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Chapter number | 9 |
Book title |
Apoptosis in Cancer Pathogenesis and Anti-cancer Therapy
|
Published in |
Advances in experimental medicine and biology, August 2016
|
DOI | 10.1007/978-3-319-39406-0_9 |
Pubmed ID | |
Book ISBNs |
978-3-31-939404-6, 978-3-31-939406-0
|
Authors |
Andreas Weigert, Javier Mora, Divya Sekar, Shahzad Syed, Bernhard Brüne |
Editors |
Christopher D. Gregory |
Abstract |
Macrophages are a group of heterogeneous cells of the innate immune system that are crucial to the initiation, progression, and resolution of inflammation. Moreover, they control tissue homeostasis in healthy tissue and command a broad sensory arsenal to detect disturbances in tissue integrity. Macrophages possess a remarkable functional plasticity to respond to irregularities and to initiate programs that allow overcoming them in order to return back to normal. Thus, macrophages kill malignant or transformed cells, rearrange extracellular matrix, take up and recycle cellular as well as molecular debris, initiate cellular growth cascades, and favor directed migration of cells. As an example, apoptotic death of bystander cells is sensed by macrophages, initiating functional responses that support all hallmarks of cancer. In this chapter, we describe how tumor cell apoptosis hijacks tumor-associated macrophages to promote tumor growth. We propose that tumor therapy should not only kill malignant cells but also target the interaction of the host with apoptotic cancer cells, as this might be efficient to limit the protumor action of apoptotic cells and boost the antitumor potential of macrophages. Leaving the apoptotic cell/macrophage interaction untouched might also limit the benefit of conventional tumor cell apoptosis-focused therapy since surviving tumor cells might receive overwhelming support by the wound healing response that apoptotic tumor cells will trigger in local macrophages, thereby enhancing tumor recurrence. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
United Kingdom | 1 | 4% |
Unknown | 27 | 96% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Student > Ph. D. Student | 6 | 21% |
Researcher | 6 | 21% |
Student > Master | 6 | 21% |
Student > Bachelor | 4 | 14% |
Student > Doctoral Student | 2 | 7% |
Other | 1 | 4% |
Unknown | 3 | 11% |
Readers by discipline | Count | As % |
---|---|---|
Biochemistry, Genetics and Molecular Biology | 8 | 29% |
Medicine and Dentistry | 7 | 25% |
Pharmacology, Toxicology and Pharmaceutical Science | 4 | 14% |
Agricultural and Biological Sciences | 3 | 11% |
Immunology and Microbiology | 1 | 4% |
Other | 1 | 4% |
Unknown | 4 | 14% |